The extent of the fattiness as assessed by ultrasonography was also higher in the H pylori-positive group.[53] There are some potential pathogenic mediators and mechanisms that contribute to the pathogenesis of NAFLD by H pylori infection, including fetuin-A, tumor necrosis factor (TNF)-α and adiponectin.[52]H pylori infection may trigger TNF-α, whereas adiponectin is secondarily increased to counterbalance the proinflammatory cascade. The gene discussed is AHSG; the disease is metabolic dysfunction-associated steatotic liver disease.